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膳食补充益生菌 SF68 通过提高丁酸盐生物利用度来增强肥胖小鼠的肠道上皮屏障功能。

Dietary Supplementation with the Probiotic SF68 Reinforces Intestinal Epithelial Barrier in Obese Mice by Improving Butyrate Bioavailability.

机构信息

Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.

Interdepartmental Research Center "Nutraceuticals and Food for Health", University of Pisa, Pisa, Italy.

出版信息

Mol Nutr Food Res. 2023 Jul;67(13):e2200442. doi: 10.1002/mnfr.202200442. Epub 2023 May 16.

DOI:10.1002/mnfr.202200442
PMID:37099449
Abstract

SCOPE

Modifications in intestinal microbiota and its metabolites, the short-chain fatty acids (SCFA) are main factors altering intestinal epithelial barrier integrity and eliciting the onset of a meta-inflammation observed in obesity. The present study is aimed at evaluating the efficacy of Enterococcus faecium (SF68) administration in counteracting the impairment of gut barrier and enteric inflammation in a model of diet-induced obesity, characterizing the molecular mechanisms underlying such beneficial effects.

METHODS AND RESULTS

Male C57BL/6J mice, fed with standard diet (SD) or high-fat diet (HFD), are treated with SF68 (10  CFU day ). After 8 weeks, plasma interleukin (IL)-1β and lipopolysaccharide binding protein (LBP) are measured, analysis of fecal microbiota composition and butyrate content as well as intestinal malondialdehyde, myeloperoxidase, mucins, tight junction protein, and butyrate transporter expression are investigated. After 8 weeks, SF68 administration counteracts the body weight gain in HFD mice, reducing plasma IL-1β and LBP. In parallel, SF68 treatment acts against the intestinal inflammation in HFD-fed animals and improves the intestinal barrier integrity and functionality in obese mice via the increase in tight junction protein and intestinal butyrate transporter (sodium-coupled monocarboxylate transporter 1 ) expression.

CONCLUSIONS

Supplementation with SF68 reduces intestinal inflammation and reinforces the enteric epithelial barrier in obese mice, improving the transport and utilization of butyrate.

摘要

范围

肠道微生物群及其代谢物的改变,即短链脂肪酸(SCFA),是改变肠道上皮屏障完整性并引发肥胖中观察到的代谢性炎症的主要因素。本研究旨在评估粪肠球菌(SF68)给药在对抗饮食诱导肥胖模型中肠道屏障损伤和肠内炎症的功效,表征这种有益作用的潜在分子机制。

方法和结果

雄性 C57BL/6J 小鼠用标准饮食(SD)或高脂肪饮食(HFD)喂养,并接受 SF68(10 CFU·天)治疗。8 周后,测量血浆白细胞介素(IL)-1β和脂多糖结合蛋白(LBP),分析粪便微生物群组成和丁酸盐含量,以及肠道丙二醛、髓过氧化物酶、粘蛋白、紧密连接蛋白和丁酸盐转运蛋白的表达。8 周后,SF68 给药可抑制 HFD 小鼠的体重增加,降低血浆 IL-1β和 LBP。同时,SF68 治疗可对抗 HFD 喂养动物的肠道炎症,并通过增加紧密连接蛋白和肠道丁酸盐转运体(钠偶联单羧酸转运体 1)表达来改善肥胖小鼠的肠道屏障完整性和功能。

结论

SF68 的补充可减少肥胖小鼠的肠道炎症并增强肠上皮屏障,改善丁酸盐的转运和利用。

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